Good news! There are so many good reasons why to drink coffee or is this a commercial dressed up as science?
"... But in their latest study, the scientists made a surprising discovery: caffeine doesn’t act on this growth switch directly. Instead, it works by activating another important system called AMPK, a cellular fuel gauge that is evolutionarily conserved in yeast and humans.
“When your cells are low on energy, AMPK kicks in to help them cope,” ... “And our results show that caffeine helps flip that switch.”
Interestingly, AMPK is also the target of metformin, a common diabetes drug that’s being studied for its potential to extend human lifespan together with rapamycin.
Longevity benefits
Using their yeast model, the researchers showed that caffeine's effect on AMPK influences how cells grow, repair their DNA, and respond to stress—all of which are tied to ageing and disease. ..."
From the abstract:
"Caffeine can modulate cell cycle progression, override DNA damage checkpoint signalling and increase chronological lifespan (CLS) in various model systems.
Early studies suggested that caffeine inhibits the phosphatidylinositol 3-kinase-related kinase (PIKK) Rad3 to override DNA damage-induced cell cycle arrest in fission yeast. We have previously suggested that caffeine modulates cell cycle progression and lifespan by inhibiting the Target of Rapamycin Complex 1 (TORC1).
Nevertheless, whether this inhibition is direct or not, has remained elusive. TORC1 controls metabolism and mitosis timing by integrating nutrients and environmental stress response (ESR) signalling. Nutritional or other stresses activate the Sty1-Ssp1-Ssp2 (AMP-activated protein kinase complex, AMPK) pathway, which inhibits TORC1 and accelerates mitosis through Sck2 inhibition. Additionally, activation of the ESR pathway can extend lifespan in fission yeast. Here, we demonstrate that caffeine indirectly activates Ssp1, Ssp2 and the AMPKβ regulatory subunit Amk2 to advance mitosis. Ssp2 is phosphorylated in an Ssp1-dependent manner following exposure to caffeine.
Furthermore, Ssp1 and Amk2, are required for resistance to caffeine under conditions of prolonged genotoxic stress. The effects of caffeine on DNA damage sensitivity are uncoupled from mitosis in AMPK pathway mutants.
We propose that caffeine interacts synergistically with other genotoxic agents to increase DNA damage sensitivity.
Our findings show that caffeine accelerates mitotic division and is beneficial for CLS through AMPK.
Direct pharmacological targeting of AMPK may serve towards healthspan and lifespan benefits beyond yeasts, given the highly conserved nature of this key regulatory cellular energy sensor."
Caffeine could slow cellular ageing: new research shows how (original news release) "A new study ... reveals how caffeine —the world’s most popular neuroactive compound—might do more than just wake you up. The study in the journal Microbial Cell shows how caffeine could play a role in slowing down the ageing process at a cellular level."
Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast (open access)
The charts in this research paper were very poorly done. This is part F of a larger chart that appears towards the end of the paper (on page 11 of 16), but it contains the summary of the study. Part F should have been a separate chart at the beginning of the article.
No comments:
Post a Comment